Browsing by Author "Moizuddin, Mohammed"
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Item A case of inclusion body myositis masquerading as statin-induced myopathy(2023) Fatima, Fariya; Quresh, Zehratul; Ansari, Mahira; Moizuddin, Mohammed; Quresh, QuretulBackground: Inclusion body myositis (IBM) is a common acquired myopathy in individuals older than 50 years of age. This idiopathic inflammatory myopathy carries an insidious progression with frequent delays in diagnosis and a high incidence of misdiagnosis resulting in significant morbidity and disability for affected individuals. Clinical features include asymmetric weakness predominantly affecting the quadriceps and/or finger flexors, and a slow, progressive course leading to loss of ambulation and dysphagia. Creatinine kinase (CK) levels are usually less than 10 times normal and erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) fall within normal limits. Myositis-specific autoantibodies are typically absent in patients with IBM; however, highly specific positive cytoplasmic 5'-nucleotidase 1A (cN1A) autoantibodies can help distinguish IBM from other forms of myositis, such as polymyositis. There is an association of IBM with autoimmune diseases, such as Sjögren's syndrome, sarcoidosis, and some lymphoproliferative disorders. Unlike many other autoimmune diseases, the condition typically affects males more frequently with a male-to-female ratio of approximately 3:1. Mean age of symptom onset ranges from 61 to 68, with over 20% of patients developing symptoms in their forties. Case presentation: A 71-year-old male patient with a long-standing history of hypertension and dyslipidemia was evaluated for complaints of progressively worsening proximal muscle weakness, fatigue, and dyspnea for more than 2 years in duration. He had been prescribed 40 mg of atorvastatin and was presumed to have statin-induced myopathy after taking the drug for 1 year. Physical examination revealed an otherwise healthy male with proximal muscle weakness with stable vital signs. CK was within normal limits and CRP was 6.6. He was noted to have a negative ANA screen extensive myositis and HMGCR antibody, but was found positive for cytoplasmic 5'-nucleotidase 1A (cN1A) autoantibodies, thus confirming suspicion of IBM. MRI of the thigh demonstrated generalized muscular atrophy with no active inflammation. Given the prolonged nature of the disease in the patient, no active inflammation was noted. He is responding well to tapering doses of steroids and other immunomodulatory options being discussed with him. Conclusion: This case illustrates the importance of appropriate recognition of IBM, and the challenges associated with diagnosis and management. This acquired myopathy may be mistaken for other conditions such as statin-induced myopathy and should be considered in the evaluation of progressive muscle weakness in individuals over 50 years of age. Appropriate intervention is essential to prevent progressive disability with rapid loss of strength and function in affected individuals.Item An Unusual Case of Metabolic Acidosis- Mind the Gap!(2024-03-21) Choi, Jonathan; Moizuddin, MohammedBackground: Euglycemic diabetic ketoacidosis (EDKA) is a rare, life-threatening condition characterized by acidosis, elevated ketone levels, and a high anion gap (AG) in the presence of normal blood glucose. We present a unique case of EDKA in a non-diabetic patient linked to sodium-glucose cotransporter-2 (SGLT2) inhibitor use. Case Presentation: A 64-year-old female with a history of chronic hypercapnic respiratory failure, Charcot-Marie-Tooth disease, hypertension, depression, and chronic diastolic congestive heart failure was admitted for progressively worsening confusion, left-sided weakness, facial numbness, dyspnea, generalized weakness and feeling ill for 24 hours duration. Physical exam revealed afebrile, confused patient with bilateral lower extremity weakness. At home she was on Dapagliflozin, Metoprolol, Sacubitril-Valsartan, and Spironolactone. Laboratory results showed a glucose level of99 mg/dl, a bicarbonate level of 13 mmol/l, an AG of 18mEq/l, delta gap of 6mEq/l, arterial pH of 7.08, and PCO2 of 36. Urinalysis revealed leukocytes, positive nitrate, high glucose (>1000 mmol/l), ketones (>80 mmol/l), and beta-hydroxybutyrate (6.7 mmol/l). Computed tomography (CT) brain scan showed no intracranial hemorrhage. EDKA was diagnosed, and her treatment included intravenous dextrose, insulin, and broad-spectrum antibiotics for a urinary tract infection. She responded well to treatment, with resolution of her metabolic acidosis. Conclusion: The incidence of EDKA due to SGLT2 inhibitors is approximately 0.1%. Timely diagnosis can be challenging due to normal glucose levels. We know that SGLT2 inhibitors enhance glycosuria, promoting ketone body production through lipolysis. Elevated glucagon and reduced glucose levels contribute to hepatic ketone production. Increasing glucagon levels and low glucose levels promote the production of ketones, and this glucagon-insulin imbalance leads to the development of EDKA. Differential diagnoses for high anion gap metabolic acidosis (HAGMA) include methanol, uremia, diabetic ketoacidosis, propylene glycol, isoniazid, iron overdose, lactic acidosis, ethylene glycol, and salicylate toxicity. Initial laboratory assessments should include basic electrolytes, glucose, calcium, magnesium, creatinine, blood urea nitrogen, serum and urine ketones, beta-hydroxybutyric acid, arterial or venous blood gas analysis, lactic acid, and complete blood count, among others. Blood cultures, urine analysis, and chest radiographs are needed to rule out any infection. High-calorie glucose infusion and tight glycemic control are key elements in ameliorating intractable metabolic acidosis brought about by SGLT2 inhibitor-induced EDKA. Remember to always mind the gap in patients with HAGMA! Healthcare providers should remain diligent, considering EDKA, especially with normal glucose levels. Patients need to be educated about the risks associated with SGLT2 inhibitors, fostering open communication and shared decision-making for safer medication management.